With an increasingly aging and stressed society, the number of patients with lower urinary tract dysfunction (LUTD) has increased. LUTD is a generic term for urine collection disorder and dysuria, and the symptoms derived from LUTD are lower urinary tract symptoms (LUTS). One of the LUTS is an overactive bladder syndrome (OABs). OABs may be generally called overactive bladder (OAB) in some cases. In any case, it is a disease defined as “a symptom syndrome which essentially has urinary urgency and which is usually accompanied by urinary frequency and nocturia. Urge urinary incontinence is not necessary”. The symptoms associated with OABs interfere with general life such as work, daily life, mental activity, and the like, and thus lower the quality of life (QOL). Currently, a first choice drug as an agent for treating OABs is an anticholinergic agent. However, it is necessary for the anticholinergic agent to be used also in due consideration of an anti-muscarinic effect such as thirst and residual urine, and thus, is not always effective for all patients (see, for example, Non-patent literature 1). Under these circumstances, there is a demand for development of a therapeutic agent which has a different mechanism from that of the anticholinergic agent (see, for example, Non-patent literature 1).
Recently, in LUTS, particularly in OABs, the role of urothelium has attracted attention. For LUTS, it has become clear that various chemical mediators are released in the urothelial cells, which cause a micturition reflex through the receptors of bladder sensory nerve terminals. Among them, one of the chemical mediators, prostaglandin E2 (PGE2), binds with a prostaglandin E receptor 1 (EP1 receptor) in the afferent nerves (especially C fibers) in the urothelium to increase the micturition reflex. In addition, PGE2 binds with the EP1 receptors present in the bladder smooth muscle to contract the bladder. In fact, it has been reported that the EP1 receptor antagonists inhibit both of the increase in the micturition reflex and the increase in the afferent nerve activities by PGE2 (see, for example, Non-patent literature 2 and Non-patent literature 3). From these, it is suggested that PGE2 is involved in contraction of the bladder smooth muscle and increase in the bladder sensory nerves through the EP1 receptors. Furthermore, it is reported that EP1 receptor antagonists do not increase the amount of the residual urine, but increase the bladder capacity (see, for example, Non-patent literature 4).
There exist four subtypes, EP2, EP3, and EP4 as well as EP1, of the PGE2 receptor. The EP1 receptor exists in the lungs as well as the bladder and the urothelium, the skeletal muscle, the renal collecting duct, and the like (see, for example, Non-patent literature 2). Therefore, it is expected that by changing the selectivity of the subtypes of the PGE2 receptor, the target organs of the drugs, or the target tissues, a therapeutic agent for desired diseases can be developed.
A compound represented by the general formula (A) is disclosed as a therapeutic drug for Alzheimer's disease (see, for example, Patent literature 1).

[wherein A1 represents -L-CO2H or the like, A2 represents a phenyl group which may have substituents, A3 and A4 independently represent a hydrogen atom, a halogen atom, an alkyl group, an alkoxy group, a haloalkyl group or a haloalkoxy group or the like, L represents —(CH2)n-(CH2)n- or —(CH2)nO(CH2)n- or the like, each n independently represents integer selected from 0 to 8].
However, there is no suggestion or disclosure that these compounds have an EP1 receptor antagonism.
As an indole derivative having an EP1 receptor antagonism, a compound represented by the chemical structural formula (B) (sodium 6-(6-chloro-3-isobutylindol-1-yl)pyridine-2-carboxylate) and a analog thereof are disclosed (see, for example, Non-patent literature 5).

However, these compounds differ from the compounds of the present invention in the chemical structural formula in terms of the position, the type, or the like of a substituent.